Changes in the Number of CD38 and CX43 Immunopositive Cells in the Neurovascular Unit of the Brain in Experimental Alzheimer’s Disease
Author:
Publisher
Pleiades Publishing Ltd
Subject
Cell Biology
Link
https://link.springer.com/content/pdf/10.1134/S1990519X22020067.pdf
Reference34 articles.
1. Alano, C.C., Tran, A., Tao, R., Ying, W., Karliner, J.S., and Swanson, R.A., Differences among cell types in NAD(+) compartmentalization: a comparison of neurons, astrocytes, and cardiac myocytes, J. Neurosci. Res., 2007, vol. 85, p. 3378. https://doi.org/10.1002/jnr.21479
2. Blacher, E., Dadali, T., Bespalko, A., Haupenthal, V.J., Grimm, M.O., Hartmann, T., Lund, F.E., Stein, R., and Levy, A., Alzheimer’s disease pathology is attenuated in a CD38-deficient mouse model, Ann. Neurol., 2015, vol. 78, p. 88. https://doi.org/10.1002/ana.24425
3. Bruzzone, S., Franco, L., Guida, L., Zocchi, E., Contini, P., Bisso, A., Usai, C., and De, Flora, A., A self-restricted CD38-connexin43 cross-talk affects NAD+ and cyclic ADP-ribose metabolism and regulates intracellular calcium in 3T3 fibroblasts, J. Biol. Chem., 2001, vol. 276, p. 48300. https://doi.org/10.1074/jbc.M107308200
4. Camacho-Pereira, J., Tarragó, M.G., Chini, C.C.S., Nin, V., Escande, C., Warner, G.M., Puranik, A.S., Schoon, R.A., Reid, J.M., Galina, A., and Chini, E.N., CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism, Cell Metab., 2016, vol. 23, p. 1127. https://doi.org/1016/j.cmet.2016.05.006
5. Chini, E.N., CD38 as a regulator of cellular NAD: a novel potential pharmacological target for metabolic conditions, Curr. Pharm. Des., 2009, vol. 15, p. 57. https://doi.org/10.2174/138161209787185788
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